Alcoholism is a multi-faced disease with many different etiologies. No single approach to treatment has been universally successful. The Charleston Alcohol Research Center at the Medical University of South Carolina has the research goal of improving treatment for people suffering from alcohol abuse and behavioral neuroscience and pharmacotherapy were assembled to a research team poised to take on the challenge of working together to identify promising new pharmacological treatments for alcoholism and its comorbid disorders. The Center funding mechanism afforded the opportunity for collaborative, and more importantly, provided the researchers both Core support and organizational infrastructure to facilitate their productivity. It also provided a source of funding for pilot projects to bring new investigators as well as new technology to the Center. The improved communication and interaction between Center investigators accomplished the expected result of attracting new investigators into the alcohol research areas as well as stimulating the acquisition of extramural funding for new and collaborative research projects. The original administrative/scientific leaders continue to occupy leadership positions, and the original five senior level researchers are involved in the renewal. These investigators are joined in their renewal projects by junior faculty or faculty new to alcohol research in a """"""""team"""""""" approach. The threat that ties all the research components together in the Center is pharmacotherapy. The projects are interdigitated as closely as possible between a human and a animal counterpart. Research Components 1 and 2 involve evaluation of medications and combinations of medications on alcohol ingestion and reward in humans and animals, respectively. Finally, Research Component 5 examines the role of stress and a medication that may act by modifying the stress response on alcohol craving in humans with comorbid alcoholism and Post Traumatic Stress Disorder. The Lopez Pilot Project is the animal counterpart to this study. In this renewal application, neuroimaging technology has been introduced to the Center, as has the acoustic startle response, electrophysiology, and molecular biology. The Charleston Alcohol Research Center is well positioned to evaluate promising compounds in animal models, in a human laboratory setting, and in clinical trials.

Agency
National Institute of Health (NIH)
Institute
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Type
Specialized Center (P50)
Project #
5P50AA010761-08
Application #
6626419
Study Section
Special Emphasis Panel (ZAA1-DD (01))
Program Officer
Huebner, Robert B
Project Start
1995-12-10
Project End
2005-11-30
Budget Start
2003-01-01
Budget End
2003-12-31
Support Year
8
Fiscal Year
2003
Total Cost
$1,928,905
Indirect Cost
Name
Medical University of South Carolina
Department
Psychiatry
Type
Schools of Medicine
DUNS #
183710748
City
Charleston
State
SC
Country
United States
Zip Code
29425
Haun, Harold L; Griffin, William C; Lopez, Marcelo F et al. (2018) Increasing Brain-Derived Neurotrophic Factor (BDNF) in medial prefrontal cortex selectively reduces excessive drinking in ethanol dependent mice. Neuropharmacology 140:35-42
Schacht, Joseph P; Voronin, Konstantin E; Randall, Patrick K et al. (2018) Dopaminergic Genetic Variation Influences Aripiprazole Effects on Alcohol Self-Administration and the Neural Response to Alcohol Cues in a Randomized Trial. Neuropsychopharmacology 43:1247-1256
McGuier, Natalie S; Rinker, Jennifer A; Cannady, Reginald et al. (2018) Identification and validation of midbrain Kcnq4 regulation of heavy alcohol consumption in rodents. Neuropharmacology 138:10-19
Nimitvilai, Sudarat; Lopez, Marcelo F; Woodward, John J (2018) Effects of monoamines on the intrinsic excitability of lateral orbitofrontal cortex neurons in alcohol-dependent and non-dependent female mice. Neuropharmacology 137:1-12
Dowdle, Logan T; Brown, Truman R; George, Mark S et al. (2018) Single pulse TMS to the DLPFC, compared to a matched sham control, induces a direct, causal increase in caudate, cingulate, and thalamic BOLD signal. Brain Stimul 11:789-796
Zamudio-Bulcock, Paula A; Homanics, Gregg E; Woodward, John J (2018) Loss of Ethanol Inhibition of N-Methyl-D-Aspartate Receptor-Mediated Currents and Plasticity of Cerebellar Synapses in Mice Expressing the GluN1(F639A) Subunit. Alcohol Clin Exp Res 42:698-705
Cannady, Reginald; Rinker, Jennifer A; Nimitvilai, Sudarat et al. (2018) Chronic Alcohol, Intrinsic Excitability, and Potassium Channels: Neuroadaptations and Drinking Behavior. Handb Exp Pharmacol 248:311
Harlan, Benjamin A; Becker, Howard C; Woodward, John J et al. (2018) Opposing actions of CRF-R1 and CB1 receptors on VTA-GABAergic plasticity following chronic exposure to ethanol. Neuropsychopharmacology 43:2064-2074
Hanlon, Colleen A; Dowdle, Logan T; Henderson, J Scott (2018) Modulating Neural Circuits with Transcranial Magnetic Stimulation: Implications for Addiction Treatment Development. Pharmacol Rev 70:661-683
Hanlon, Colleen A; Dowdle, Logan T; Gibson, Nicole B et al. (2018) Cortical substrates of cue-reactivity in multiple substance dependent populations: transdiagnostic relevance of the medial prefrontal cortex. Transl Psychiatry 8:186

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